Kay-Dietrich Wagner

A possible role for atrial fibroblasts in postinfarction bradycardia.

The Wilms' tumor gene Wt1 is required for normal development of the retina.

The Wilms' tumor suppressor Wt1 is expressed in the coronary vasculature after myocardial infarction.

Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats.

The Wilms' tumor suppressor Wt1 is associated with the differentiation of retinoblastoma cells.

Transgenic overexpression of the sarcoplasmic reticulum Ca2+ATPase improves reticular Ca2+ handling in normal and diabetic rat hearts.

Time-dependent changes of the susceptibility of cardiac contractile function to hypoxia-reoxygenation after myocardial infarction in rats.

The Wilms' tumor suppressor Wt1 encodes a transcriptional activator of the class IV POU-domain factor Pou4f2 (Brn-3b).

The complex life of WT1.

Cardiac fibroblasts and the mechano-electric feedback mechanism in healthy and diseased hearts.

The long-lasting impact of postnatal neuropeptide Y.

Oxygen-regulated expression of the Wilms' tumor suppressor Wt1 involves hypoxia-inducible factor-1 (HIF-1).

Mechanically induced potentials in atrial fibroblasts from rat hearts are sensitive to hypoxia/reoxygenation.

Characterization of stretch-activated ion currents in isolated atrial myocytes from human hearts.

1,25-dihydroxyvitamin D3-induced apoptosis of retinoblastoma cells is associated with reciprocal changes of Bcl-2 and bax.

The major podocyte protein nephrin is transcriptionally activated by the Wilms' tumor suppressor WT1.

A splice variant of the Wilms' tumour suppressor Wt1 is required for normal development of the olfactory system.

Coronary vessel development requires activation of the TrkB neurotrophin receptor by the Wilms' tumor transcription factor Wt1.

Intermediate filament protein nestin is expressed in developing kidney and heart and might be regulated by the Wilms' tumor suppressor Wt1.

An inducible mouse model for PAX2-dependent glomerular disease: insights into a complex pathogenesis.

The Wilms tumor suppressor Wt1 promotes cell adhesion through transcriptional activation of the alpha4integrin gene.

The Wilms' tumor suppressor WT1 is associated with melanoma proliferation.

A novel Wilms' tumor 1 gene mutation in a child with severe renal dysfunction and persistent renal blastema.

Role of the Wilms' tumour transcription factor, Wt1, in blood vessel formation.

Peroxisome proliferator-activated receptor beta stimulation induces rapid cardiac growth and angiogenesis via direct activation of calcineurin.

Peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) acts as regulator of metabolism linked to multiple cellular functions.

Enhanced L-type calcium currents in cardiomyocytes from transgenic rats overexpressing SERCA2a.

The podocyte protein nephrin is required for cardiac vessel formation.

Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) is highly expressed in liposarcoma and promotes migration and proliferation.

The Telomeric Protein TRF2 Regulates Angiogenesis by Binding and Activating the PDGFRβ Promoter.

The Wilms' tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression.

RNA Activation of the Vascular Endothelial Growth Factor Gene (VEGF) Promoter by Double-Stranded RNA and Hypoxia: Role of Noncoding VEGF Promoter Transcripts.

Inducible Conditional Vascular-Specific Overexpression of Peroxisome Proliferator-Activated Receptor Beta/Delta Leads to Rapid Cardiac Hypertrophy.

Dnmt2/Trdmt1 as Mediator of RNA Polymerase II Transcriptional Activity in Cardiac Growth.

TRF2 acts as a transcriptional regulator in tumor angiogenesis.

Small RNA-directed epigenetic programming of embryonic stem cell cardiac differentiation.

The differential spatiotemporal expression pattern of shelterin genes throughout lifespan.

CDK9 Regulates Apoptosis of Myoblast Cells by Modulation of microRNA-1 Expression.

Coronary Artery Formation Is Driven by Localized Expression of R-spondin3.

Andersen's syndrome mutants produce a knockdown of inwardly rectifying K(+) channel in mouse skeletal muscle in vivo.